Oncotarget

Research Papers:

miR-29 regulates Tet1 expression and contributes to early differentiation of mouse ESCs

Yanhua Cui, Ting Li, Dehua Yang, Song Li and Weidong Le _

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Oncotarget. 2016; 7:64932-64941. https://doi.org/10.18632/oncotarget.10751

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Abstract

Yanhua Cui1,*, Ting Li2,*, Dehua Yang2, Song Li1, Weidong Le1,2,3

1Center for Translational Research on Neurological Diseases, the First Affiliated Hospital, Dalian Medical University, Dalian, China

2Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China

3Collaborative Innovation Center for Brain Science, the First Affiliated Hospital, Dalian Medical University, Dalian, China

*These authors contributed equally to this work

Correspondence to:

Weidong Le, email: wdle@sibs.ac.cn

Keywords: Tet1, 5hmC, embryonic stem cells, miR-29 family

Received: April 11, 2016     Accepted: June 30, 2016     Published: July 21, 2016

ABSTRACT

The ten-eleven translocation-1 (Tet1), which converts 5-methylcytosine (5mC) to 5-hydroxymethycytosine (5hmC), plays important roles in many important biological processes, such as mouse embryonic stem cells (ESCs) maintenance. However, the mechanisms for Tet-1 regulation remain largely unknown. Here we showed that miR-29 family (miR-29a, miR-29b and miR-29c) can directly repress Tet1 expression. We found that Tet1 was highly expressed and 5hmC was presented at relatively high levels in mouse ESCs, but the levels of both Tet1 and 5hmC were reduced during the early differentiation of ESCs. On the contrary, miR-29 level was increased in this process. ESCs stably transfecting with miR-29 precursors showed lower levels of Tet1 protein and 5hmC. Furthermore, we demonstrated that miR-29 overexpression selectively affected cell lineage markers and skewed ESC differentiation, which was similar in Tet1 knockdown ESCs. Our results indicate that miR-29 is a direct regulator of Tet1 in mouse ESCs.


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